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Academic Background

Ingolf Bach carried out his doctoral work at the Pasteur Institute in Paris, supported by the Boehringer Ingelheim Foundation. He received his Ph.D. in 1993 from the University of Paris VII. Supported by fellowships from EMBO and HFSPO, he was a post-doctoral fellow from 1993 to 1996 and, later, an Assistant Research Biologist at the University of California, San Diego. From 1998 to 2005, he was an Assistant Professor and Heisenberg Scholar at the Center for Molecular Neurobiology at the University of Hamburg. Dr. Bach joined the Program in Gene Function and Expression at the University of Massachusetts Medical School as an Associate Professor in June of 2005.

Neuronal Cell Fate Specification

Photo: Ingolf Bach, Ph.D.

A fundamental question in biology is how protein complexes consisting of multiple proteins regulate basic biological processes such as embryogenesis and, when disturbed, cause human disease. Our research investigates molecular mechanisms by which LIM domain proteins and associated cofactors regulate differential gene expression during cell fate specification events.

The LIM domain mediates protein-protein interactions and is found in various proteins including LIM homeodomain transcription factors (LIM-HD), LIM-only (LMO) proteins and LIM kinases (LIMK). We are particularly interested in functions and regulation of LIM-HD proteins that specify cell lineages and regulate neuronal differentiation and brain morphogenesis during vertebrate and invertebrate development. The biological activity of LIM-HDs is regulated by LIM domain-associated cofactors CLIM/Lbd and RLIM/Rnf12. These cofactors are widely expressed and also exert important functions in the mammary gland and during X chromosome inactivation in female mice.

To carry out our studies we apply molecular, biochemical and genetic methods using mouse development as model system. Current research projects in the laboratory comprise studies on the roles of LIM domain proteins / associated cofactors 1) for cell fate decisions during nervous system development, 2) for X chromosome inactivation, and 3) for mammary gland development, differentiation and breast cancer. Results of this research are intended to illuminate mechanisms of how cell fate decisions are orchestrated and how disturbances can lead to human disease.

One or more keywords matched the following items that are connected to Bach, Ingolf
Item TypeName
Academic Article Functional characterization of the gene encoding RLIM, the corepressor of LIM homeodomain factors.
Academic Article Two members of an HNF1 homeoprotein family are expressed in human liver.
Academic Article Cloning of human hepatic nuclear factor 1 (HNF1) and chromosomal localization of its gene in man and mouse.
Academic Article Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice.
Academic Article Paternal RLIM/Rnf12 is a survival factor for milk-producing alveolar cells.
Academic Article Releasing the break on X chromosome inactivation: Rnf12/RLIM targets REX1 for degradation.
Concept Chromosomes, Human, Pair 17
Concept Chromosomes, Human, Pair 12
Concept X Chromosome Inactivation
Concept Chromosome Mapping
Concept X Chromosome
Academic Article RLIM is dispensable for X-chromosome inactivation in the mouse embryonic epiblast.
Academic Article Impaired imprinted X chromosome inactivation is responsible for the skewed sex ratio following in vitro fertilization.
Academic Article Regulation of X-linked gene expression during early mouse development by Rlim.
Academic Article Rlim-Dependent and -Independent Pathways for X Chromosome Inactivation in Female ESCs.
Academic Article Rlim/Rnf12, Rex1, and X Chromosome Inactivation.
Academic Article Roles of the Rlim-Rex1 axis during X chromosome inactivation in mice.
Academic Article How does the Xist activator Rlim/Rnf12 regulate Xist expression?
Search Criteria
  • Chromosomes Human Pair 2